Mood Disorders I and II Flashcards
What is the criteria for Major Depresison Disorder?
* Must be SAD or express ANHADONIA (loss of interest/pleasure), or irritability if a child + 4 additional symptoms
(5 out of 9 total WITHOUT it being due to a medical condition or due to direct physiological effects of a substance)
S: saddness
I: decreased interest/pleasure
G: guilt / feelings of worthlessness
E: decreased Energy / fatigue
C: decreased concentration / indecisiveness
A: decreased appetite / wt loss
P: psychomotor agitation or retardation (observed by others)
S: suicidal thoughts
S: change in sleep (insomnia or hypersomnia)
Risk Factors for MDD:
gender preference:
peak age onset:
genetics?
ethnic preference:
other?
Risk Factors for MDD:
gender preference: Women > men (2:1) – changes post-menopausal
peak age onset: 20-30s
genetics? moderate genetic risk (if one parent 10-15% chance, 2 parents 20-10% chance, MZ twins 50%, DZ twins 15-20%)
genetic cluster regarding family history (genetics, psychological and environmental disruptions)
ethnic preference: Higher in hispanic women and American Indians; lower in AA males, asians
other? single, divorced, widowed, negative childhood (loss, neglect, abuse)
income, profession, religion, geography have minimal impact
Is this a single event episode, multiple? chronic?
with INC # of events –> increased risk.
ppl with 1 event - 50%
2 events - 70%
3+ 95%
For most its a reoccuring CHRONIC illness, with tiggers to relapse over time are less and less (will just come back withouth triggers = stress vulnerability model)
How do people develop MDD? (5)
- Genetic predisposition - SMALLER hippocampus, abnormal serotonin transport protein (now can be measured through genetic testing)
- Poor physiological coping strageies or skills - secondary to trauma, loss, dysfunction, societal situations, lack of resiliency..
- Triggering events - biological (MEDS! substances, diseases), psychological, environmental
- Change in brain processes that cause us to interpret external or internal stimuli in different ways - negative cognitions, pessimisms, physical changes, withdrawal, retreat, lack of rewards, altered self awareness
- Symptoms that hinger our ability to reach our previous neurobiological homeostasis via neurogenesis through enrichment – social connections; inability to return to normal due to difficult in making/keeping social connections, exercise, new learning
MDD is a ________ brain disorder.
Although we don’t have a biological marker, the closest marker is a theory based on chronic ____ [low/high] level _____ [dec/inc] of _______ [hormone] secondary to stress –> causing disruption in healthy neurogenesis and may add to neurodegeneration.
MDD is a NEURODEGENERATIVE brain disorder.
Although we don’t have a biological marker, the closest marker is a theory based on chronic LOW level INCREASES of CORTISOLsecondary to stress –> causing disruption in healthy neurogenesis and may add to neurodegeneration.
What three monoamines have been implicated in depression?
NE, DA and SE
especially serotonin!
What are the three major theories explaining the pathophysiology of MDD?
- Inflammatory theory
- Structural theory
- Network theory
Explain the inflammatory theory of MDD:
Low levels of chronic inflammation from either reactive illness* (lupus, CAD) or *persistent heightened level of corticosteriods from stress produce a toxic inflammatory milieu where neurodegeneration INC and neurgenesis is inhibited.
It is though that IL 6 (interfers with serotonin metabolism) might be the main culprit
Thought that cytokines released also can lead to higher risk for heart disease and Alzheimers. HYPERSECRETION of cortisol can cause acute and more severe depression (Cushing’s disease)
Explain the structural theory of MDD:
Depression is caused by abnormal changes in brain areas that can be identified premorbidly and are exacerbated in active illness.
Atrophy of the prefrontal cortex, amygdala and hippocampus, AND enlargement of the insula and anterior cingulated cortex
Enhancing neurogenesis in those areas that are atrophied or altering GABA in the insual are areas of exploration
Explain the Network Hypothesis for MDD:
NOt a specific altered brain area that leads to depression but aberrancies in the TRACTS between the areas. White matter abnormalities in tracts between the MEDIAL PREFRONTAL CORTEX, AMYGDALA and HIPPOCAMPUS.
Glucose activity is DEC in the hippocampus and dorsalateral prefrontal cortex and INC in the amygdala, ventral striatum and subgenual cingulate gyrus
Thought that depression is a result of miscommunication and misinterpretation of various brain regions involved with interpreting emotions
- Depression will only improve if neurogenesis can occur in those tracts to retun the interaction and perception to normal*
- Abnormalities can be seen in various neuroimaging, show less activity at limbic system and prefronta alreasy of focus*
What can depression be a risk factor for (4):
- More major depression! The longer the depression the greater the chornicity of illness. If <6 months 60% chance of remission; if > 24 months, 10-15% chance of remission
- Other co-morbid psychiatric illnesses (60%) of the time - Etoh and anxiety diorders most common
- Cardiac events (due to cytokines and inflammation )
- CNS - CVA, parksonism, demetia, seizures, strokes, Alzheimers
Other conditions that may cause or mimic major depression: (4)
- Psychosocial - loss, abandonment, lack of nuturing, emptiness, anger towards inward, developmental arrest at a dependent stage with a disordered parten, low self-estmee, failures, lack of self object stability, consistency
- Environment - poverty, deaths, famine, wars, oppresison, abuse, torture, drugs, learned helplessness, side effects of meds, chemical toxins, ID, medical conditions
- Other medical conditions - **once the condition is stable the depressive symptoms should dissipate** examples: EBV (mono) – fatigue, decreased mood….; infectious, neoplasms (pancreatic CA, brain tumors, lymphomas), endocrime (hyper/hypo thyroidims, hypo/hyperadrenocortical function - Cushing’s and Addison’s), diabetes; Metabolic/nutritional (uremia, pellagra, anemia), Neurologica (frontaltemporal dementia, Parkinson’s Huntington’s subdural hematoma, temporal lobe epileps, MS, head trauma)
- Substance/medication-induced - corticosteroids, BC, antipsychotics, interferons, RESERPINE, isotretinoin (Accutane), beta blockers, central actinv anti-hypertensives, all of the pschoactive substances (alcohol, cocaine, marijuana, opioids, sedatives/hypnotics)
What are examples of “specifiers” that can be added to a dx in order to better quialify them and lead to better/more appropriate treatment:
MD with…
anxious distress
mixed features (anxiety and sadness)
melancholic features (worse in teh AM, terminal insomnia, excessive guilt, marked wt loss, total lack of pleasure-anhedonia)
atypical features (wt gain, over sensitive mood reactivity, oversleeping, leaden paralysis - feel like can’t move arms or legs)
mood congruent psychotic features (about 10% of epidoses- hallucinations and delusions that have depressive contentn “i feel like I am rotting and the devil is telling me bad things”
mood in-congruent psychotic features
catatonia
peripartum onset
seasonal pattern
Persistent Depressed Disorder
Duration:
Depressed mood for:
Symptoms (6):
Tx:
Persistent Depressed Disorder
Duration: 2 YEARS, has never been symptoms free for longer than 2 months
Depressed mood for: most of the day on more days than not, course tends to be non-remitting; can have MDD ON TOP of this disorder
Symptoms (6): TWO of the SIX
- poor appetite or overeating
- low energy or fatigue
- insomnia or hypersomnia
- poor concentration or difficult decision making
- feelings of hopelessness
Tx: difficult to treat
Premenstrural Dysphoric Disorder
Duration:
SX: (11 total)
In the MAJORITY of menstrual cycles, symtoms occurin during the final week before start of menstruation, and as soon as period comes, goes away within 2-3 days.
Causes significant distress or impairment
NOT an exacerbation of another similar disorder (ie-MDD)
AT LEAST ONE of the following:
Marked affective lability
Marked irritability and anger or interpersonal conflicts
Marked depressed mood, feelings or hopelessness
Marked anxiety, tension and/or feelings on edge
AND at least ONE of the following:
DEC interest
Poor concentration
Lethargy
Change in appetite
Hyperinsomnia or insomnia
Sense of being out of control
Physical symptoms-breast tenderness, bloating, mus pain
*A TOTAL OF 5 or MORE symptoms
MDD + melancholia:
SX (5)
TX
Tests?
MDD symptoms AND also:
- lack of reactivity of any pleasureable situaiton
- early AM mood worse
- early morning awakening
marked agitation or retardation
- excessive guilt
Rx: Anti-depressions!
Test: dexamethasone Suppression Test (DST) usually positive unable to supress cortical levels
Atypical MDD:
- oversleeping
- overeating
- leaden paralysis
- interpersonal sensitivity
- mood reactivity, leading to roller-coaster type of mood
MDD Psychotic
SX (3)
RX
10% of all MDD
- MDD features but also presence of psychotic element*
- Nihilism (no future, world will end)
- deflusions “I am bad” “I have cancer-rotting in me”
- hallucinations, usually negative, usually AUDITORY
RX: anti-psychotic or ECT essential!
newer SSRIs may not work welll
Need to R/O bipolar, and schizophrenia!
Seasonal MDD:
SX
RX
20% of people at this latitude have a seasonal mood fluctuations
SX- similar to atypical depression but patients tend to become “HYPER IN SUMMER” while October - February is bad
RX: light therapy of some help, anti-depressants just as effective
Bereavement/grief VS MDD
Bereavement, for most people, is normal life reaction. Will have many of the same symptoms as MDD but individual can still experience pleasure and joy at times. However, loses are a precipitant of MDD and one should not hesitate to treat as MDD if symptoms are severe enough. Don’t wait and normalize - longer the delay of treatment, worse depression can get
expectations are that by 3 months, many of hte symptoms have resolved and the person moves on a bit more with their life
Adjustment disorder with depressed mood:
= Some signs of depression that cause clinical concern but with an acute stressor that occurred within 3 months o_f the onset of symptoms_
Tx: brief therapy or social interventions are all that’s needed
Criteria for other disorders are NOT MET and the symptoms abate by 6 months after the end of the stressor
Special populations that require extra attention:
ELDERLY!
New incident rate increases >65 y/o
Males have a high rate of suicide
SX: often masked depression, they are irritable, a_ngry, don’t care, often somatic in presentation, don’t try, may be confused with dementia (pseudodementia)_
RX: treatable
TEENAGERS:
Hard because many times teenagers are not familiar with what depresison is and how it looks or feels; we may dismiss the teenager as “bad teens” - yet look for behavioral changes. High suicide rate (they don’t know whats going on)
What is the criteria needed to be diagnosed with Bipolar I Disorder:
Requires at least ONE MANIC episode although most commonly there will be episdoes of major depression an dother mood states in the the history
MANIC espidoes:
- Distinct period of abnormally and persistent elevated, expansive or irritable mood present for most of the day for at least ONE WEEK
AND 3 (or 4 if the mood is only irritable) of the following symptoms
- inflated self-esteem or grandiosity
- decreased need for sleep
- More talkative than usual or pressure to keep talking
- flight of ideas / subjective experience of racing thoughts
- distractibility
- INC in goal-directive activities or psychomotor agitation
- Excessive involvement in pleasurable actvities that have a high potential for painful consequences (buying, speeding, sexual indiscretions, foolish business ventures)
*Marked impairment in functioning in job, social activities or relationships with others or there are psychotic features
*symptoms NOT caused by a substance or medical condition
Bipolar individuals:
____ % of the time will be spent in a depressive phase
____ % spent in hypmanic or manic phase
____ % spent in the euthymic state (normal, non-depressed, reasonably positive individual)
When bipolar individuals are in their euthymic phases, do they have normal functioning, back to baseline?
Does their lifespan change?
Is there an increased risk for suicide?
What is a main causitive factor for some of these changes?
Bipolar individuals:
40-45 % of the time will be spent in a depressive phase
5-10 % spent in hypomanic or manic phase
45 % spent in the euthymic state (normal, non-depressed, reasonably positive individual)
When bipolar individuals are in their euthymic phases, do they have normal functioning, back to baseline? No - there is evidence of brain function abnormalities, processing abilities are impaired, verbal memory, attention and executive functioning are less than baseline.
Does their lifespan change? 8-10 years less primarily due to metabolic syndrome co-morbidies
Is there an increased risk for suicide? 15-20X higher
What is a main causitive factor for some of these changes? their insight into their illness is always suspect leading to issues of substance abuse, non-compliance with medications and treatment, and potentially challenging live courses
